The overall goal of the proposal is to explore immunopathogenetic mechanisms in experimental and human renal disease and to attempt to modify selectively the immune responses in ways that may prevent or diminish the renal damage. In particular, we will study cellular and structural features of models of cell-mediated glomerular reactions produced by transfer of syngeneic lymphocytes from sensitized donors to rats with glomerular bound antigens, investigate the role of cell mediated mechanisms and the importance of antigens on tubular cells in the pathogenesis of experimental anti-TBM nephritis, explore further the mechanisms by which transferred anti-TBM antibodies can stimulate auto-anti-TBM antibody production in guinea pigs (autoimmune amplification), study the ways by which anti-idiotype antibodies suppress experimental anti-TBM nephritis and investigate the role of autoantibodies against glomerular constituents in the pathogenesis of Heymann nephritis and human membranous glomerulonephritis.